Implementation and Impact of a Store-and-Forward Teledermatology Platform in an Urban Academic Safety-Net Health Care System.

Background:Minority and low-income patients disproportionately experience dermatologic access challenges. Store-and-forward (SAF) teledermatology has emerged as a model of care delivery that may improve access. We sought to evaluate patterns of utilization and overall impact after SAF teledermatology implementation in a safety-net health care system. Methods:We performed a retrospective review of 3,285 teledermatology consultations from 2014 to 2017 in an urban academic safety-net health care system. Results:A total of 1,680 (51.2%) patients were referred for inflammatory/rash conditions and 967 (29.5%) for skin lesions. The teledermatologist recommended in-person evaluation in 1,199 encounters (36.5%). Median wait time for a subsequent appointment was 36 days (range 0-244 days). Of subsequent in-clinic visits, 237 patients (26.4%) underwent skin biopsy. No-show rate after referral was 11.8%. In comparison, median wait time for dermatology appointment through standard referral was 64 days, with a no-show rate of 18.6%. Biopsy rate of patients referred via teledermatology was 26.4%, in comparison to a rate of 10.9% of patients referred directly from primary care provider. Discussion:Implementation of SAF teledermatology in a safety-net health system resulted in avoidance of 63.5% potential dermatology visits. Consultation typically resulted in a change in suspected diagnosis or management plan. Rates of concordance between teledermatology consults and in-person evaluations were high. Median wait time was reduced by almost half, no-show rate was reduced ∼37%, and biopsy rate was more than double for teledermatology patients compared with standard referral. Conclusion:These findings suggest that SAF teledermatology may improve access to high-quality dermatologic care and increase clinic efficiencies for patients in safety-net health care systems.

Treatment of metastatic cutaneous Crohn disease with certolizumab.

Metastatic Crohn disease is a rare cutaneous manifestation of Crohn disease characterized by granulomatous lesions discontinuous with the diseased areas of the gastrointestinal tract. We report a case of a 32-year-old woman with history of Crohn disease who was admitted for treatment of cellulitis after presenting with a tender erythematous plaque of the left calf. Microbiological tests including tissue cultures were negative. A skin biopsy revealed granulomatous dermatitis consistent with metastatic cutaneous Crohn disease. Owing to concomitant perianal fistulas and abscesses and prior infusion reaction to infliximab, the patient was treated with certolizumab, a pegylated tumor necrosis factor (TNF) inhibitor combined with methotrexate resulting in complete resolution of the skin lesion. This case emphasizes the importance of recognizing this rare skin manifestation of Crohn disease and adds certolizumab as one of TNF inhibitors useful in the treatment of metastatic cutaneous Crohn disease.

Tobacco smoke-induced immunologic changes may contribute to oral carcinogenesis.

OBJECTIVE: The objective of this study was to determine if tobacco smoke (TS), a risk factor for cancers of the aerodigestive tract, may contribute to oral carcinogenesis, in part, by suppressing local immunity. METHODS: Mice were placed in Plexiglas holders in which they breathed TS through the nose and mouth for 1 hour daily for 21 days. Control mice breathed room air in the same manner. One day after the last exposure, mice were immunized by application of oxazolone to each buccal mucosa. Control mice were mock immunized by application of vehicle alone. Five days later, all mice were challenged on the ears with oxazolone, and 24-hour ear swelling assessed as contact hypersensitivity. RESULTS: Mice exposed to TS had a significantly smaller contact hypersensitivity response compared with controls. When subsequently reimmunized on the glabrous skin, mice originally primed through TS-exposed mucosa could not be fully immunized, indicating induction of immunologic tolerance by exposure to hapten through TS-perturbed mucosa. Immunocompetent mice exposed to TS in this manner and challenged by submucosal placement of a syngeneic malignant tumor had significantly increased tumor growth over time compared with controls. No difference in growth rate was observed when the experiment was performed with natural killer cell-deficient, SCID (severe combined immunodeficiency) mice. In addition, exposure of epidermal Langerhans cells in vitro to an aqueous extract of TS impaired their ability to undergo maturation and to present antigen to responsive T cells. CONCLUSIONS: Immunologic changes induced in the oral cavity by exposure to TS may play a role in the development of oral cancers.

N-acetyl-S-farnesyl-l-cysteine suppresses chemokine production by human dermal microvascular endothelial cells.

Isoprenylcysteine (IPC) molecules modulate G-protein-coupled receptor signalling. The archetype of this class is N-acetyl-S-farnesyl-l-cysteine (AFC). Topical application of AFC locally inhibits skin inflammation and elicitation of contact hypersensitivity in vivo. However, the mechanism of these anti-inflammatory effects is not well understood. Dermal microvascular endothelial cells (ECs) are involved in inflammation, in part, by secreting cytokines that recruit inflammatory cells. We have previously shown that the sympathetic nerve cotransmitter adenosine-5'-triphosphate (ATP) and adenosine-5'-O-(3-thio) triphosphate (ATPγS), an ATP analogue that is resistant to hydrolysis, increase secretion of the chemokines CXCL8 (interleukin-8), CCL2 (monocyte chemotactic protein-1) and CXCL1 (growth-regulated oncogene α) by dermal microvascular ECs. Production of these chemokines can also be induced by the exposure to the proinflammatory cytokine TNFα. We have now demonstrated that AFC dose-dependently inhibits ATP-, ATPγS- and TNFα-induced production of CXCL1, CXCL8 and CCL2 by a human dermal microvascular EC line (HMEC-1) in vitro under conditions that do not affect cell viability. Inhibition of ATPγS- or TNFα-stimulated release of these chemokines was associated with reduced mRNA levels. N-acetyl-S-geranyl-l-cysteine, an IPC analogue that is inactive in inhibiting G-protein-coupled signalling, had greatly reduced ability to suppress stimulated chemokine production. AFC may exert its anti-inflammatory effects through the inhibition of chemokine production by stimulated ECs.